Understand how your body defends itself against an almost infinite variety of pathogens with this comprehensive immune system flashcard deck. The immune system is one of the most complex and fascinating systems in biology — and understanding it is essential fo...
Understand how your body defends itself against an almost infinite variety of pathogens with this comprehensive immune system flashcard deck. The immune system is one of the most complex and fascinating systems in biology — and understanding it is essential for medicine,
pharmacology, and public health.
This deck covers physical and chemical barriers (first line of defence), the innate immune response (inflammation, phagocytosis, natural killer cells), and the adaptive immune response (B lymphocytes, T lymphocytes, antibodies, clonal selection and expansion,
immunological memory, vaccines, and active vs passive immunity). Also covers autoimmune diseases, allergies, and HIV/AIDS. Essential for GCSE, A-Level, AP Biology, and university immunology courses.
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1st line (physical/chemical barriers): Skin, mucus, cilia, stomach acid, tears, saliva. 2nd line (innate/non-specific): Inflammation, phagocytosis, fever, natural killer cells. 3rd line (adaptive/specific): B and T lymphocytes, antibodies, immunological memory.
A rapid, non-specific response present from birth. Responds the same way to any pathogen. Components: physical barriers, phagocytes (neutrophils, macrophages), natural killer cells, complement proteins, inflammation, fever. Does not produce lasting immunity or memory.
A slow (days), specific response tailored to a particular antigen. Involves lymphocytes (B and T cells). Produces immunological memory — faster and stronger response upon re-exposure to the same antigen. Acquired over time.
Any molecule (usually a protein or polysaccharide) on the surface of a pathogen (or any foreign substance) that triggers an immune response. Each pathogen has unique antigens. The immune system learns to recognize "self" antigens and targets "non-self" antigens.
The process by which phagocytes (neutrophils, macrophages) engulf and destroy pathogens. Steps: Chemotaxis (attracted to infection site) → Recognition (pathogen surface antigens bind to phagocyte receptors) → Engulfment (pseudopodia surround pathogen → phagosome) → Digestion (lysosomes fuse → enzymes destroy pathogen).
White blood cells produced and matured in the bone marrow. Each B cell has unique surface receptors recognizing a specific antigen. When activated, B cells differentiate into plasma cells (secrete antibodies) and memory B cells (long-lived; rapid response on re-exposure).
White blood cells produced in bone marrow and matured in the thymus. Types: T helper cells (CD4⁺): Activate B cells, cytotoxic T cells, and macrophages — coordinate the immune response. Cytotoxic T cells (CD8⁺): Kill virus-infected cells and cancer cells directly. Regulatory T cells: Suppress excessive immune responses.
A Y-shaped glycoprotein produced by plasma cells. Has two variable regions (antigen-binding sites) — specific to one antigen. Structure: two heavy chains + two light chains. Five classes: IgG, IgA, IgM, IgD, IgE.
Neutralization: Bind to and block toxins or viral surface proteins. Agglutination: Clump pathogens together → easier for phagocytes to engulf. Opsonization: Coat pathogens → signal phagocytes to engulf them. Complement activation: Trigger complement proteins → lyse bacterial membranes.
Each lymphocyte has unique receptors for one specific antigen. When an antigen enters the body, it selects and activates the lymphocyte(s) with matching receptors. Those cells rapidly divide (clonal expansion) → large population of identical cells all targeting that one antigen.
After the primary immune response, long-lived memory B and T cells persist in the body. On re-exposure to the same antigen: memory cells are activated rapidly → much faster, stronger, and longer-lasting secondary response — often eliminating the pathogen before symptoms occur.
Primary response: First exposure — slow (7–14 days), low antibody levels as lymphocytes are selected and multiplied. Secondary response: Re-exposure — rapid (1–3 days), much higher antibody levels, longer-lasting. Due to memory cells. The basis of vaccines.
A preparation containing weakened/killed pathogens, their antigens, or toxoids (inactivated toxins). Stimulates a primary immune response without causing disease → creates immunological memory. On real infection, memory cells produce rapid secondary response → disease prevented or mild.
Active immunity: Body produces its own antibodies and memory cells — long-lasting. Natural (infection) or artificial (vaccination). Passive immunity: Pre-formed antibodies received from another organism — immediate but short-lived (no memory). Natural: maternal antibodies via placenta/breast milk. Artificial: antivenom, immunoglobulin therapy.
When a sufficiently high proportion of a population is immune (through infection or vaccination), the spread of disease is limited and even unimmunised individuals are protected. The required percentage varies by pathogen's R₀ value — for measles it is ~95%.
A condition where the immune system incorrectly attacks the body's own healthy tissues. Examples: Type 1 diabetes (attacks pancreatic beta cells), rheumatoid arthritis (attacks joints), multiple sclerosis (attacks myelin sheaths), lupus (attacks multiple organs). Caused by failure of self-tolerance mechanisms.
An exaggerated immune response to a harmless antigen (allergen). IgE antibodies are produced on first exposure → bind to mast cells. On re-exposure, allergen cross-links IgE → mast cells release histamine → inflammation, mucus, vasodilation, bronchoconstriction. Treated with antihistamines. Anaphylaxis = severe, life-threatening allergic reaction.
A cascade of ~30 plasma proteins that are activated by pathogens, leading to: Opsonization (coating pathogens for phagocytosis), Chemotaxis (attracting phagocytes), Membrane Attack Complex (MAC) formation — punching holes in bacterial membranes → bacterial lysis. Part of innate immunity but can be activated by antibodies (adaptive link).
Cell-surface glycoproteins that present antigen fragments to T cells. MHC class I (all nucleated cells): Present intracellular antigens (e.g., viral peptides) to cytotoxic T cells → infected cells killed. MHC class II (antigen-presenting cells — macrophages, dendritic cells, B cells): Present extracellular antigens to T helper cells.
A non-specific response to tissue damage or infection. Signs: Redness (vasodilation), heat (increased blood flow), swelling (increased permeability → fluid leaks out), pain (prostaglandins stimulate nociceptors). Function: increases blood flow, brings immune cells to the site, creates hostile environment for pathogens.
Lymphocytes of the innate immune system that kill virus-infected cells and tumour cells without needing prior sensitization (unlike cytotoxic T cells). They detect cells with abnormal or missing MHC class I molecules (sign of infection or cancer) → release perforin and granzymes → cell apoptosis.
Monoclonal antibodies are identical antibodies produced from a single clone of B cells (hybridoma technology). Medical uses: Cancer treatment (target tumour antigens — e.g., trastuzumab/Herceptin for breast cancer), Autoimmune diseases (e.g., infliximab for rheumatoid arthritis), Pregnancy tests (detect hCG), COVID-19 treatment.
A state where the immune system is weakened or absent. Primary: Genetic — e.g., Severe Combined Immunodeficiency (SCID — "bubble boy disease"). Secondary (acquired): Caused by external factors — HIV/AIDS, chemotherapy, malnutrition, organ transplant immunosuppression. Results in vulnerability to opportunistic infections.
Proteins secreted by virus-infected cells that warn neighbouring cells of viral infection. They induce nearby cells to produce antiviral proteins, inhibit viral replication, activate NK cells, and upregulate MHC expression. Part of the innate immune response — act before specific immunity develops.